Again the study showed that phosphorylation of IKK-β was increased in diabetes, but the blockade of NF-κB, oxidative stress, and the genetic deletion of TNF-α attenuated phosphorylation of IKK-β, suggesting that the phosphorylation of IKK-β is increased in diabetic mice by the activation of oxidative stress and TNF-α [33]. The gene discussed is NFKB1; the disease is diabetes mellitus.